A 48 year-old male with hypertension and hyperlipidemia presents with headache. Notes onset of symptoms 8 hours prior to presentation, reaching maximal severity within seconds. Headache improved with over-the-counter analgesics. On examination, there are no neurological deficits, neck is supple. A CT head non-contrast is obtained:

ED Course:

A lumbar puncture is performed, CSF sampling reveals xanthochromia – neurosurgery is consulted and the patient is admitted for angiography and possible intervention.

An Algorithm for the Evaluation of Headache

High-Risk Historical Features

• Sudden onset (seconds/minutes), patient recalls activity at onset
• Worst in life or change in character from established headache
• Fever, neck pain/stiffness
• Altered mental status
• Malignancy
• Coagulopathy: iatrogenic, hepatopathy, dialysis
• Immunocompromised
• Rare: CO exposure, jaw claudication, PCKD

Location of Pain

1. Unilateral: migraine
2. Periorbital: glaucoma, CVT, optic neuritis, cluster
3. Facial/maxillary: trigeminal neuralgia, sinusitis
4. Temporal: GCA
5. Occipital: cerebellar stroke
6. Nuchal: meningitis

Characteristics of Primary Headaches

Physical Examination Findings

Vital Signs

Fever: present in 95% of patients with meningitis

Head

Trauma: signs of basilar skull fracture

Temporal artery tenderness/induration: GCA

Pericranial muscle tenderness: tension headache

Trigger point, Tinnel sign: occipital neuralgia

Eyes

Pupillary defects: aneurysm with CN III compression

Papilledema, absence of spontaneous venous pulsations: elevated intracranial pressure

EOM abnormalities: ICH, mass lesion, neuropathy (DM, Lyme)

Horner syndrome (ptosis, miosis, anhidrosis): carotid dissection

Visual field defect: stroke, atypical migraine

Conjunctival injection: glaucoma (fixed, mid-size pupil, elevated intraocular pressure), cluster headache

Mouth

Thrush: immunocompromise

Sinuses

Tenderness to palpation, abnormal transillumination: sinusitis

Neck

Resistance to supine neck flexion: meningitis

Kernig: supine position, hip flexed, knee flexed, resistance to knee extension

Brudzinski: supine position, neck flexion results in knee flexion

Jolt accentuation: patient rotates head side-to-side, 2-3 times/sec exacerbates headache

References:

1. Russi, C. (2013). Headache. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 170-175). Elsevier Health Sciences.
2. Godwin SA, Villa J. “Acute headache in the ED: Evidence-Based Evaluation and Treatment Options.” Emerg Med Pract 2001; 3(6): 1-32.
3. Edlow, J. A., Panagos, P. D., Godwin, S. A., Thomas, T. L., & Decker, W. W. (2008). Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Annals of emergency medicine, 52(4), 407–436. doi:10.1016/j.annemergmed.2008.07.001
4. WikEM: Headache

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Brief HPI:

A 66-year-old male with a history of hypertension, diabetes, hyperlipidemia and prior stroke presents with acute-onset right-sided numbness. Examination demonstrates decreased sensation to light touch and pinprick in right upper- and-lower extremities as well as right face. Strength, cranial nerve and cerebellar testing is normal.

Discussion:

Infarction of the ventral posterolateral nucleus of the thalamus disrupts relays from the medial lemniscus and spinatholamic tracts extending to the cortex.

Case 2

Brief HPI:

A 34-year-old female with no significant medical history presents with headache and neck pain. Examination is notable for decreased strength with decreased sensation to pinprick (and preserved light touch) in bilateral upper extremities.

Discussion:

The central cord lesion affects the adjacent, medial fibers of the corticospinal tract resulting in upper extremity weakness. Disruption of crossing spinothalamic tract fibers results in diminished pain and temperature sensation at the level of the lesion.

Anatomy^3,4

Sensory information is gathered from specialized receptors in skin and soft-tissues which detect a variety of stimuli including temperature, pressure, vibration, and pain. This is subsequently transmitted through peripheral nerves which in certain regions coalesce into larger bundles before entering the spinal cord through the dorsal nerve root. Upon entering the spinal cord, sensory information is divided into two tracts:

1. Spinothalamic: Small, poorly-myelinated fibers carrying pain, temperature and touch stimuli synapse with second-order neurons over several levels in the ipsilateral dorsal horn crossing to the contralateral side in the anterior commissure anterior to the central canal. Touch information ascends in the anterior spinothalamic tract while pain and temperature information ascends in the lateral spinothalamic tract.
2. Dorsal column: Large, myelinated fibers carrying vibration and proprioception information ascend in the ipsilateral posteromedial spinal cord. Fibers from the thoracic and lumbar region occupy the more medial (gracile) column, while fibers from the cervical region occupy the more lateral (cuneate) column. These fibers synapse in their respective nuclei in the medulla before crossing to the contralateral medial lemniscus.

Both tracts proceed to the ventral posterolateral (VPL) nucleus of the thalamus, through the internal capsule before terminating in the somatotopically-arranged primary somatosensory cortex in the parietal lobe.

Understanding the neuroanatomy supports a systematic approach to the evaluation of sensory disturbances. It is important to note that the transmission of light touch sensation involves both pathways and offers less localizing value when compared to specific assessment of proprioception or pain detection. Sensory disturbances are often accompanied by motor abnormalities  which can further aid with localization. Other key distinguishing features include acuity of onset wherein abrupt presentations may suggest ischemia or infarction, compared to more indolent processes with broader differentials (including compressive mass lesions, demyelination, or autoimmune disease).

An Algorithm for the Evaluation of Sensory Disturbances⁵

References

1. Case courtesy of Dr Bruno Di Muzio, Radiopaedia.org, rID: 45066
2. Case courtesy of Dr Bahman Rasuli, Radiopaedia.org, rID: 65655
3. Aminoff MJ. Numbness, Tingling, and Sensory Loss. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 19e New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com/content.aspx?bookid=1130&sectionid=79724797. Accessed February 07, 2020.
4. Sensory Disorders. In: Simon RP, Aminoff MJ, Greenberg DA. eds. Clinical Neurology, 10e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=2274&sectionid=176234164. Accessed February 07, 2020.
5. Berkowitz AL. Numbness: A Localization-Based Approach. In: McKean SC, Ross JJ, Dressler DD, Scheurer DB. eds. Principles and Practice of Hospital Medicine, 2e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=1872&sectionid=146977205. Accessed February 07, 2020.

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An approximately 70 year-old male with unknown medical history is brought to the emergency department with altered mental status. A community member contacted police after not seeing the patient for the past three days which was unusual. Upon entering the patient’s home, EMS found the patient on the ground, unresponsive. Capillary glucose was normal and naloxone was administered without appreciable effect.

On arrival in the emergency department, the patient remained unresponsive to verbal and noxious stimulation and was intubated for airway protection. Vital signs were notable for hypotension (BP 88/45mmHg) and a core temperature of 96.5°F. Physical examination demonstrated cool extremities and ecchymosis and edema involving the right upper and lower extremities. The patient’s blood pressure improved with fluid resuscitation and empiric broad-spectrum antibiotics were administered due to concern for infection in the setting of hypothermia.

Laboratory/Imaging Results

Laboratory tests were notable for leukocytosis and creatine kinase above the threshold for detection. Radiology preliminary interpretation of non-contrast head imaging was normal. A lumbar puncture was performed with grossly purulent cerebrospinal fluid.

Hospital Course

The patient was admitted for the treatment of presumed meningitis. Radiology final interpretation of non-contrast head computed tomography commented on ventricular debris suggestive of ventriculitis which was later confirmed on magnetic resonance imaging^1,2. Due to poor response to systemic antibiotics, neurosurgery was consulted, a ventricular drain was placed with administration of intrathecal antibiotics. The patient’s condition continued to deteriorate and family members elected to allow his natural death.

An Algorithm for the Analysis of Cerebrospinal Fluid (CSF)^3-14

References

1. Lesourd A, Magne N, Soares A, et al. Primary bacterial ventriculitis in adults, an emergent diagnosis challenge: report of a meningoccal case and review of the literature. BMC Infect Dis. 2018;18(1):226. doi:10.1186/s12879-018-3119-4.
2. Gofman N, To K, Whitman M, Garcia-Morales E. Successful treatment of ventriculitis caused by Pseudomonas aeruginosa and carbapenem-resistant Klebsiella pneumoniae with i.v. ceftazidime-avibactam and intrathecal amikacin. Am J Health Syst Pharm. 2018;75(13):953-957. doi:10.2146/ajhp170632.
3. Dorsett M, Liang SY. Diagnosis and Treatment of Central Nervous System Infections in the Emergency Department. Emerg Med Clin North Am. 2016;34(4):917-942. doi:10.1016/j.emc.2016.06.013.
4. Perry JJ, Alyahya B, Sivilotti MLA, et al. Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage: prospective cohort study. BMJ. 2015;350:h568. doi:10.1136/bmj.h568.
5. Lee SCM, Lueck CJ. Cerebrospinal fluid pressure in adults. J Neuroophthalmol. 2014;34(3):278-283. doi:10.1097/WNO.0000000000000155.
6. Brouwer MC, Thwaites GE, Tunkel AR, van de Beek D. Dilemmas in the diagnosis of acute community-acquired bacterial meningitis. Lancet. 2012;380(9854):1684-1692. doi:10.1016/S0140-6736(12)61185-4.
7. Wright BLC, Lai JTF, Sinclair AJ. Cerebrospinal fluid and lumbar puncture: a practical review. J Neurol. 2012;259(8):1530-1545. doi:10.1007/s00415-012-6413-x.
8. Gorchynski J, Oman J, Newton T. Interpretation of traumatic lumbar punctures in the setting of possible subarachnoid hemorrhage: who can be safely discharged? Cal J Emerg Med. 2007;8(1):3-7.
9. Deisenhammer F, Bartos A, Egg R, et al. Guidelines on routine cerebrospinal fluid analysis. Report from an EFNS task force. Eur J Neurol. 2006;13(9):913-922. doi:10.1111/j.1468-1331.2006.01493.x.
10. Seehusen DA, Reeves MM, Fomin DA. Cerebrospinal fluid analysis. Am Fam Physician. 2003;68(6):1103-1108.
11. Shah KH, Edlow JA. Distinguishing traumatic lumbar puncture from true subarachnoid hemorrhage. J Emerg Med. 2002;23(1):67-74.
12. Walker HK, Hall WD, Hurst JW. Clinical Methods: The History, Physical, and Laboratory Examinations. 1990.
13. Mayefsky JH, Roghmann KJ. Determination of leukocytosis in traumatic spinal tap specimens. Am J Med. 1987;82(6):1175-1181.
14. Geiseler PJ, Nelson KE, Levin S, Reddi KT, Moses VK. Community-acquired purulent meningitis: a review of 1,316 cases during the antibiotic era, 1954-1976. Rev Infect Dis. 1980;2(5):725-745.

The post Cerebrospinal Fluid appeared first on Differential Diagnosis of.

An approximately 60 year-old male with a history of hypertension and diabetes is brought to the emergency department after noting difficulty speaking and right-sided weakness upon awakening. Prehospital capillary glucose measured 268mg/dL. He went to sleep at 10pm on the evening prior to presentation.

The patient arrives in the emergency department awake and alert at 9am. He was unable to provide history due to speech difficulty but is able to follow commands. Examination demonstrates right upper and lower extremity weakness. Computed tomography of the head and neck is obtained, non-contrast imaging shows no hemorrhage and angiography demonstrates left MCA occlusion. He proceeds emergently to the angiography suite where mechanical thrombectomy restores normal perfusion. The patient is discharged to an inpatient rehabilitation facility for intensive physical therapy three days later.

CT Angiography

Code Stroke Algorithm

References

1. Goldstein LB, Simel DL. Is this patient having a stroke? JAMA. 2005;293(19):2391-2402. doi:10.1001/jama.293.19.2391.
2. Hemmen TM, Meyer BC, McClean TL, Lyden PD. Identification of nonischemic stroke mimics among 411 code strokes at the University of California, San Diego, Stroke Center. J Stroke Cerebrovasc Dis. 2008;17(1):23-25. doi:10.1016/j.jstrokecerebrovasdis.2007.09.008.
3. Prabhakaran S, Ruff I, Bernstein RA. Acute stroke intervention: a systematic review. JAMA. 2015;313(14):1451-1462. doi:10.1001/jama.2015.3058.
4. Yew KS, Cheng EM. Diagnosis of acute stroke. Am Fam Physician. 2015;91(8):528-536.
5. Hemphill JC, Greenberg SM, Anderson CS, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2015;46(7):2032-2060. doi:10.1161/STR.0000000000000069.
6. Hankey GJ. Stroke. Lancet. 2017;389(10069):641-654. doi:10.1016/S0140-6736(16)30962-X.
7. Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2018;49(3):e46-e110. doi:10.1161/STR.0000000000000158.
8. Hasan TF, Rabinstein AA, Middlebrooks EH, et al. Diagnosis and Management of Acute Ischemic Stroke. Mayo Clin Proc. 2018;93(4):523-538. doi:10.1016/j.mayocp.2018.02.013.
9. Thomalla G, Simonsen CZ, Boutitie F, et al. MRI-Guided Thrombolysis for Stroke with Unknown Time of Onset. N Engl J Med. 2018;379(7):611-622. doi:10.1056/NEJMoa1804355.

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A 72 year-old male with a history of hypertension and hiatal hernia presents to the emergency department with one week of generalized weakness. His family report decreased oral intake with frequent emesis over the past four days. He denies chest pain, shortness of breath, abdominal pain, or other complaints. During the interview he has a generalized tonic-clonic seizure which persists for five minutes despite the administration of 4mg of lorazepam.

An Algorithm for the Management of Seizures

The management of active seizures is algorithmic, starting with a rapid assessment of airway patency, supporting ventilation (with appropriate positioning, nasopharyngeal airway adjuncts and bag-valve mask if needed) and ensuring adequate perfusion. Patients should have continuous vital sign monitoring, supplemental oxygen to maintain oxygen saturation >92% and intravenous access¹.

Pharmacologic treatment follows a stepwise approach, detailed in the algorithm below. The focus is on immediate stabilization and progressively escalating anti-epileptic drugs eventually requiring endotracheal intubation and continuous infusions of sedatives^2-4.

Pathophysiology

Seizures are caused by excessive and disorganized neuronal activation, typically induced by global alterations in the production and transmission of impulses (electrolyte derangements, drugs/toxins, infection), or foci of increased irritability (hemorrhage, stroke, mass) – a pathophysiologic motif that mimics cardiac tachyarrhythmias (sympathomimetic toxicity or scarred myocardium for example)¹. Status epilepticus, defined as a seizure lasting greater than five minutes or recurrent seizures without a return to normal baseline, shares an equally high short-term mortality – greater than 20%⁵.

Syncope vs. Seizure

The algorithm below details historical and examination features that may assist with distinguishing epileptic seizure from non-epileptic activity^6,7.

Case Conclusion

The patient continued to seize and a point-of-care chemistry panel revealed a serum sodium of 108mEq/L. Seizures abate after the infusion of hypertonic saline (100mL of 3% saline over 10 minutes, repeated until cessation of seizures). While hyponatremia is generally corrected slowly – owing to the risk of osmotic demyelination – immediate correction in this setting is critical⁸.

The remainder of the patient’s evaluation demonstrated urine osmolarity is 389mOsm/kg and urine sodium is 53mmol/L, in the setting of relative euvolemia on examination these findings were consistent with SIADH. Head computed tomography is obtained and reveals a sellar mass.

View Hyponatremia Algorithm

References

1. McMullan JT, Davitt AM, Pollack CV Jr. Seizures. In: Rosen’s Emergency Medicine. Mosby Incorporated; 2002:2808. doi:10.1016/S1474-4422(06)70350-7.
2. Billington M, Kandalaft OR, Aisiku IP. Adult Status Epilepticus: A Review of the Prehospital and Emergency Department Management. J Clin Med. 2016;5(9):74. doi:10.3390/jcm5090074.
3. Huff JS, Morris DL, Kothari RU, Gibbs MA, Emergency Medicine Seizure Study Group. Emergency department management of patients with seizures: a multicenter study. Academic Emergency Medicine. 2001;8(6):622-628.
4. Prasad M, Krishnan PR, Sequeira R, Al-Roomi K. Anticonvulsant therapy for status epilepticus. Prasad M, ed. Cochrane Database Syst Rev. 2014;16(9):CD003723. doi:10.1002/14651858.CD003723.pub3.
5. Logroscino G, Hesdorffer DC, Cascino G, Annegers JF, Hauser WA. Short-term mortality after a first episode of status epilepticus. Epilepsia. 1997;38(12):1344-1349.
6. Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol. 2002;40(1):142-148.
7. McKeon A, Vaughan C, Delanty N. Seizure versus syncope. Lancet Neurol. 2006;5(2):171-180. doi:10.1016/S1474-4422(06)70350-7.
8. Goh KP. Management of hyponatremia. Am Fam Physician. 2004;69(10):2387-2394.

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Algorithm for the Evaluation of Weakness

Upper Versus Lower Motor Neuron Findings

Comparison Between Myopathy, Neuropathy and Neuromuscular Junction Processes

References

1. Ganti L, Rastogi V. Acute Generalized Weakness. Emerg Med Clin North Am. 2016;34(4):795-809. doi:10.1016/j.emc.2016.06.006.
2. Asimos AW. Weakness: A Systematic Approach To Acute, Non-traumatic, Neurologic And Neuromuscular Causes. Emergency Medicine Practice. 2002;4(12):1-28.
3. Morchi R. Weakness. In: Rosen’s Emergency Medicine. Elsevier Inc.; 2014:2521.

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A young male with no past medical history presents to the emergency department after assault. He was punched multiple times in the face and has since noted double vision, worse with upward gaze. Examination revealed right peri-orbital edema with associated limitation to upward gaze.

Imaging:

Extraocular Muscle Actions:

Affected Anatomic Sites in Diplopia:

Coordinated eye positioning is affected by voluntary movements (requiring cranial nerve control for conjugate eye movements), vergence (for depth adjustments), as well as reflexive adjustments for head movement (requiring vestibular input). As with any motor activity, neuromuscular control must be normal with unrestricted movement of the globe within the orbit.

Algorithm for the Evaluation of Diplopia:

Diplopia has been explored previously on ddxof. The earlier algorithm was focused on identifying the paretic nerve. This algorithm uses features of the history and physical examination to identify potential etiologic causes of diplopia.

References:

1. Rucker JC, Tomsak RL. Binocular diplopia. A practical approach. Neurologist. 2005;11(2):98-110. doi:10.1097/01.nrl.0000156318.80903.b1.
2. Friedman DI. Pearls: diplopia. Semin Neurol. 2010;30(1):54-65. doi:10.1055/s-0029-1244995.
3. Alves M, Miranda A, Narciso MR, Mieiro L, Fonseca T. Diplopia: a diagnostic challenge with common and rare etiologies. Am J Case Rep. 2015;16:220-223. doi:10.12659/AJCR.893134.
4. Dinkin M. Diagnostic approach to diplopia. Continuum (Minneap Minn). 2014;20(4 Neuro-ophthalmology):942-965. doi:10.1212/01.CON.0000453310.52390.58.
5. Marx J, Walls R, Hockberger R. Rosen’s Emergency Medicine – Concepts and Clinical Practice. 8 ed. Elsevier Health Sciences; 2013:176-183.
6. Nazerian P, Vanni S, Tarocchi C, et al. Causes of diplopia in the emergency department: diagnostic accuracy of clinical assessment and of head computed tomography. Eur J Emerg Med. 2014;21(2):118-124. doi:10.1097/MEJ.0b013e3283636120.
7. Low L, Shah W, MacEwen CJ. Double vision. BMJ. 2015;351:h5385. doi:10.1136/bmj.h5385.
8. Danchaivijitr C, Kennard C. Diplopia and eye movement disorders. J Neurol Neurosurg Psychiatry. 2004;75 Suppl 4:iv24-iv31. doi:10.1136/jnnp.2004.053413.
9. Huff JS, Austin EW. Neuro-Ophthalmology in Emergency Medicine. Emerg Med Clin North Am. 2016;34(4):967-986. doi:10.1016/j.emc.2016.06.016.

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58 year-old female with no known past medical history, brought to emergency department by husband due to fatigue and weakness. The patient does not speak and cannot provide history. Her husband describes a progressive decline from normal baseline two weeks ago, noting lethargy/fatigue. Noted decreased speech and attention one week ago, and absent speech and requiring assistance with ambulation for the past two days. Thorough review of systems unremarkable excepting vomiting with decreased oral intake (tolerating fluids) and prior headache which resolved.

On examination, vital signs were normal, the patient was lying in bed and in no acute distress. The patient was non-verbal and did not follow commands (GCS E4-M5-V2). She was unable to comply with a thorough neurological examination, however pupils were equal and reactive, eyes tracked without nystagmus, no facial asymmetry noted, reflexes 1+ and symmetric in UE/LE, cannot participate in strength/sensory testing. Abdominal examination notable for infraumbilical and left-sided mass which elicits groans with palpation, though no rigidity or guarding. Mucous membranes moist, no skin tenting.

Labs

• CBC: 13.5 (97% neutrophils) , 12.9, 38.2, 240
• BMP: 107, 2.4, 70, 28, 9, 10, 0.44, 102
• Serum osmolarity: 224
• Urine osmolarity: 239
• UNa: 20

Imaging

Hospital Course

The patient was admitted to the medical intensive care unit. The following problem list details findings from the extensive inpatient evaluation.

#Altered Mental Status: The patient’s dramatically depressed level of consciousness improved gradually with correction of hyponatremia and the patient was alert, oriented and at baseline at the time of discharge. Evaluation included MRI brain which showed only chronic microvascular changes. A lumbar puncture was notable for isolated elevation of CSF protein. The patient was treated empirically for HSV encephalitis until CSF HSV PCR resulted negative. Neurology was consulted and identified increased CSF oligoclonal bands of unclear significance.

#Hyponatremia: Nephrology consulted, presumed SIADH based on urine studies (secondary to infection or malignancy). Corrected upon discharge.

#Pelvic Mass: Initially thought to arise from small bowel on CT abdomen/pelvis, after bladder decompression and transvaginal ultrasound, thought to arise from adnexa. Gynecology consulted, cyst characteristics (homogenous, fluid-filled) suggest benign process and tumor markers within normal limits. No acute intervention, drainage or biopsy warranted.

#Bladder distension: Unclear etiology, associated with mild/moderate hydronephrosis. Thought to be secondary to bladder outlet obstruction secondary to pelvic mass. Indwelling catheter placed, discontinued prior to discharge with successful spontaneous voiding trial and normal post-void residual.

Hyponatremia Applied

Altered Mental Status Applied

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Distinguishing Central vs. Peripheral Vertigo

Causes of Vertigo

Characteristics of common causes of vertigo

History

• Onset, duration, timing, severity, exacerbating factors
• Vascular risk factors: age, male, HTN, CAD, DM, atrial fibrillation
• Vestibulotoxic medications: aminoglycosides, AED

Key Physical Examination Findings

• VS: Presence of hypotension suggests presyncope
• Head: Examine for evidence of trauma
• Neck: Auscultate for carotid bruit
• Ear: Effusion or perforation suggests peripheral process (possible perilymphatic fistula)
• Eye: Examine for pupillary defects (CNIII), papilledema, extraoccular muscles
• Neuro: Cerebellar testing

Positional Testing

Dix-Hallpike

Turn head 45°

Upright sitting → supine (head overhanging bed)

Positive: nystagmus + symptoms on one side

Roll

Supine

Turn head 90°

Positive: nystagmus + symptoms on both sides, more severe on affected

HINTS¹

Normal head impulse, direction-changing nystagmus, or skew deviation suggests stroke.

Head impulse

Focus on examiner’s nose

Rapidly turn head 10° in horizontal plan

Presence of corrective saccade suggests defect of peripheral vestibular nerve

Nystagmus

Peripheral: Horizontal, unidirectional. Increases on gaze in direction of fast phase (decreases or resolves opposite)

Central: Direction changing

Skew deviation

Cross cover

Presence of vertical disconjugate gaze suggests brainstem dysfunction

HINTS Gallery

Labs

• Glucose
• CBC/Chemistry
• ECG

Imaging

• Warranted if findings concerning for central process
• MRI preferred

Management

Specific etiologies

Vestibular neuronitis: steroids

Meniere: dietary changes

BPPV: canalith repositioning

Symptomatic relief

Promethazine (Phenergan) 12.5-25mg PO

Ondansetron (Zofran) 4mg IV

Lorazepam (Ativan) 1-2mg PO/IV

Meclizine (Antivert) 25mg PO q6-8h PRN

References

1. Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y.-H., & Newman-Toker, D. E. (2009). HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke; a journal of cerebral circulation, 40(11), 3504–3510. doi:10.1161/STROKEAHA.109.551234
2. Chang, A., & Olshaker, J. (2013). Dizziness and Vertigo. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 162-169). Elsevier Health Sciences.

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Seizure

Pathologic neuronal activation leading to abnormal function

Epilepsy

Recurrent unprovoked seizures

Classification

• Cause
  • Primary: Unprovoked
  • Secondary: Provoked, caused by trauma, illness, intoxication, metabolic disturbances, etc.
• Effect on mentation
  • Generalized: involvement of both hemispheres with associated loss of consciousness (tonic-clonic, absence, atonic, myoclonic)
  • Focal: Involving single hemisphere with preserved level of consciousness
• Status epilepticus
  • Witnessed convulsions lasting >5min
  • Recurrent seizure without recovery from postictal period

Causes of Seizures

Management of Seizures

Medications for Treatment of Seizures

History

Points suggestive of seizure over alternative process

Abrupt onset

Duration < 120s

LOC

Purposeless activity: automatisms, tonic-clonic

Provocation: fever in children, substance withdrawal

Postictal state

Retrograde amnesia

Incontinence, oral trauma (buccal maceration, tongue laceration)

Rapidly resolving lactic acidosis

Important historical points for patients with seizure history

Recent illness

Medications (adherence, changes, interactions)

Substance use

Ictogenic factors

Recent/remote head trauma

Developmental abnormalities

Substance use

Sleep deprivation

Pregnancy

Key Physical Examination Findings

• Vital sign abnormalities persisting beyond immediate postictal state (may suggest drug/toxin exposure, CNS lesion)
• Nuchal rigidity
• Signs of IVDA
• Sequela
  • Head trauma
  • Tongue laceration
  • Shoulder dislocation (posterior)
• Neurological exam
  • Stroke
  • Elevated ICP
  • Failure to note improvement in postictal confusion (encephalopathy, subclinical seizures)

Labs

• Glucose
• BMP (Na, Ca, Mg)
• AED levels
• CBC (leukocytosis and bandemia common post-seizure)
• CSF
• B-hCG
• LFT (hepatic dysfunction, alcoholic hepatitis)
• Lactate (rapidly resolves on repeat)

Indications for Imaging

• New seizures
• History of trauma
• History of malignancy
• Immunocompromised
• Headache
• Anti-coagulation
• Focal neurological exam
• Persistent AMS

References

1. McMullan, J., Davitt, A., & Pollack, C. (2013). Seizures. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 156-161). Elsevier Health Sciences
2. WikEM: Seizure

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